W

1.
Epinephrine
–
Epinephrine, also known as adrenalin or adrenaline, is a hormone, neurotransmitter and medication. Epinephrine is normally produced by both the adrenal glands and certain neurons and it plays an important role in the fight-or-flight response by increasing blood flow to muscles, output of the heart, pupil dilation, and blood sugar. It does this by binding to alpha and beta receptors and it is found in many animals and some one cell organisms. Jokichi Takamine first isolated epinephrine in 1901, as a medication it is used to treat a number of conditions, including anaphylaxis, cardiac arrest, and superficial bleeding. Inhaled epinephrine may be used to improve the symptoms of croup and it may also be used for asthma when other treatments are not effective. It is given intravenously, by injection into a muscle, by inhalation, common side effects include shakiness, anxiety, and sweating. A fast heart rate and high pressure may occur. Occasionally it may result in a heart rhythm. While the safety of its use during pregnancy and breastfeeding is unclear, the adrenal medulla is a minor contributor to total circulating catecholamines, though it contributes over 90% of circulating epinephrine. Little epinephrine is found in tissues, mostly in scattered chromaffin cells. Following adrenalectomy, epinephrine disappears below the limit in the blood stream. The adrenals contribute about 7% of circulating norepinephrine, most of which is a spill over from neurotransmission with little activity as a hormone, pharmacological doses of epinephrine stimulate α1, α2, β1, β2, and β3 adrenoceptors of the sympathetic nervous system. Sympathetic nerve receptors are classified as adrenergic, based on their responsiveness to adrenaline, the term adrenergic is often misinterpreted in that the main sympathetic neurotransmitter is norepinephrine, rather than epinephrine, as discovered by Ulf von Euler in 1946. Epinephrine does have a β2 adrenoceptor-mediated effect on metabolism and the airway, the concept of the adrenal medulla and the sympathetic nervous system being involved in the flight, fight and fright response was originally proposed by Cannon. But the adrenal medulla, in contrast to the cortex, is not required for survival. In adrenalectomized patients hemodynamic and metabolic responses to such as hypoglycemia. One physiological stimulus to epinephrine secretion is exercise and this was first demonstrated using the denervated pupil of a cat as an assay, later confirmed using a biological assay on urine samples. Biochemical methods for measuring catecholamines in plasma were published from 1950 onwards, the development of extraction methods and enzyme-isotope derivate radio-enzymatic assays transformed the analysis down to a sensitivity of 1 pg for epinephrine

2.
Brasofensine
–
Brasofensine is a phenyltropane that had been under development for the treatment of Parkinsons and Alzheimers disease. In animal models of Parkinsons disease, brasofensine was effective in stimulating LMA, the isomerization of brasofensine is not between the alpha and beta positions on the 2 position of the tropane ring but rather the E/Z isomerization of the imine. It was believed that this occurs in vivo although it cannot be ruled out as a possibility that some isomerization also occurs prior to ingestion. NS-2214 is not particularly stable and is readily metabolized, for humans, most of the 14C was detected in the urine, whereas for rats as much as 80% of the 14C was in their feces. It is well known that a Schiff base is more stable than a regular imine, imine formation is a reversible process, and in the study by Zhu et al. none of the aldehyde was recovered/detected by GC-MS. Instead, the products were N-demethyl metabolites. The ester was first reduced to the alcohol, then oxidized to the aldehyde, methods have been reported for the direct reduction of esters to aldehydes, however in practice there has been some difficulty in effecting this transformation. Following this, Swern oxidation was employed to obtain the corresponding aldehyde

3.
Cocaine
–
Cocaine, also known as coke, is a strong stimulant mostly used as a recreational drug. It is commonly snorted, inhaled, or injected into the veins, mental effects may include loss of contact with reality, an intense feeling of happiness, or agitation. Physical symptoms may include a fast heart rate, sweating, high doses can result in very high blood pressure or body temperature. Effects begin within seconds to minutes of use and last between five and ninety minutes, Cocaine has a small number of accepted medical uses such as numbing and decreasing bleeding during nasal surgery. Cocaine is addictive due to its effect on the pathway in the brain. After a short period of use, there is a risk that dependence will occur. Its use also increases the risk of stroke, myocardial infarction, lung problems in those who smoke it, blood infections, Cocaine sold on the street is commonly mixed with local anesthetics, cornstarch, quinine, or sugar which can result in additional toxicity. Following repeated doses a person may have decreased ability to feel pleasure, Cocaine acts by inhibiting the reuptake of serotonin, norepinephrine, and dopamine. This results in concentrations of these three neurotransmitters in the brain. It can easily cross the barrier and may lead to the breakdown of the barrier. Cocaine is made from the leaves of the plant which are mostly grown in South America. In 2013,419 kilograms were produced legally and it is estimated that the illegal market for cocaine is 100 to 500 billion USD each year. With further processing crack cocaine can be produced from cocaine, after cannabis, cocaine is the most frequently used illegal drug globally. Between 14 and 21 million people use the drug each year, use is highest in North America followed by Europe and South America. Between one and three percent of people in the world have used cocaine at some point in their life. In 2013 cocaine use resulted in 4,300 deaths. The leaves of the plant have been used by Peruvians since ancient times. Cocaine was first isolated from the leaves in 1860, since 1961 the international Single Convention on Narcotic Drugs has required countries to make recreational use of cocaine a crime

4.
Ethylphenidate
–
Ethylphenidate is a psychostimulant and a close analog of methylphenidate. There have been reports of a perforated septum resulting from even just a few uses of ethylphenidate by insufflation. This is almost certainly due to ethylphenidate being caustic or containing caustic impurities, ethylphenidate metabolizes into methylphenidate and ritalinic acid. Tiny amounts of ethylphenidate can be formed in vivo when ethanol and methylphenidate are coingested, ethylphenidate formation appears to be more common when large quantities of methylphenidate and alcohol are consumed at the same time, such as in non-medical use or overdose scenarios. Additionally, only a few percent of the consumed methylphenidate is converted to ethylphenidate and this carboxylesterase-dependent transesterification process is also known to occur when cocaine and alcohol are consumed together, forming cocaethylene. All available data on ethylphenidates pharmacokinetics are drawn from studies conducted on rodents and its dopaminergic pharmacodynamic profile is nearly identical to methylphenidate, and is primarily responsible for its euphoric and reinforcing effects. The eudysmic ratio for ethylphenidate is superior to that of methylphenidate, the following is ethylphenidates binding profile in the mouse, alongside methylphenidates. Ethylphenidate is not explicitly controlled in US but it could possibly be considered an analog of a Schedule II substance under the Federal Analog Act if sold for human consumption, ethylphenidate is illegal in Sweden as of 15 December 2012. As a result of this, they requested that the TCDO be extended a year from 26 June 2016. Ethylphenidate is illegal in Jersey under the Misuse of Drugs Law 1978, australian state and federal legislation contains provisions that mean that analogues of controlled drugs are also covered by the legislation. Ethylphenidate would be an analogue of methylphenidate under this legislation, ethylphenidate is not controlled in Canada under the Controlled Drugs and Substances Act as the inclusion of methylphenidate in Schedule III only bans salts, not analogues. 3, 4-Dichloromethylphenidate HDEP-28 HDMP-28 Naphthylisopropylamine Naphyrone 2β-Propanoyl-3β--tropane Isopropylphenidate Propylphenidate Cocaethylene Methylphenidate Ethanol

5.
Levomethamphetamine
–
Levomethamphetamine is the levorotary form of methamphetamine. Levomethamphetamine is a sympathomimetic vasoconstrictor which is the ingredient in some over-the-counter nasal decongestant inhalers in the United States. It does not possess the potential for euphoria or addiction that dextromethamphetamine possesses, among its physiological effects are the vasoconstriction that makes it useful for nasal decongestion. The elimination half-life of levomethamphetamine is between 13.3 and 15 hours, whereas dextromethamphetamine has a half-life of about 10.5 hours, levomethamphetamine is the chemical precursor of the antiparkinsons drug selegiline. Selegiline, a monoamine oxidase B inhibitor at low doses, is also metabolized into levomethamphetamine and levoamphetamine. This has caused users to test positive for amphetamines, central side effects may include anxiety, insomnia, and anorexia. The study did not test the oral administration of levomethamphetamine, levomethamphetamine can register on urine drug screens as either methamphetamine, amphetamine, or both, depending on the subjects metabolism and dosage. L-methamphetamine metabolizes completely into L-amphetamine after a period of time

6.
Mazindol
–
Mazindol is a stimulant drug of the tetracyclic chemical class which is used as an anorectic. It was developed by Sandoz-Wander in the 1960s, mazindol is not currently available as a commercially marketed and FDA regulated prescription agent for the treatment of obesity. Mazindol is an amine, which is similar to amphetamine. It stimulates the nervous system, which increases heart rate and blood pressure. Sympathomimetic anoretics are used in the treatment of obesity. Their appetite-reducing effect tends to decrease after a few weeks of treatment, because of this, these medicines are useful only during the first few weeks of a weight-loss program. Although the mechanism of action of the sympathomimetics in the treatment of obesity is not fully known, like other sympathomimetic appetite suppressants, mazindol is thought to act as a reuptake inhibitor of norepinephrine. In addition, it inhibits dopamine and serotonin reuptake, symptoms of a mazindol overdose include, restlessness, tremor, rapid breathing, confusion, hallucinations, panic, aggressiveness, nausea, vomiting, diarrhea, an irregular heartbeat, and seizures. From considering the attached QSAR table we can make the apparent observations, Desoxylation of the alcohol in mazindol improves DAT. The compound now behaves as a functional SNDRI instead of predominantly a noradrenaline reuptake inhibitor, removal of the p-chloro atom in mazindol means that the compound now only behaves as a noradrenaline reuptake inhibitor. Changing the size of the imidazoline type ring system in mazindol to the corresponding six-membered homolog increases potency of the resultant compound at the DAT by approximately ten-fold, to make the six membered analog, one can simply substitute 1, 2-diaminoethane with 1, 3-diaminopropane. Importantly, another procedure was also published, given the data in the above table, one might also be interested in making the desoxy-mazindol analog. The synthesis for this is facile, although mazindane is relatively stable in air, it is readily oxidized to mazindol upon contact with monoamine oxidaze enzymes present at the DAT. Preparation starts by reaction of a substituted benzoylbenzoic acid with ethylenediamine The product 3 can be rationalized as being an aminal from the initially formed monoamide 2 and this is then subjected to reduction with LiAlH4 and-without isolation-air oxidation. Reduction probably proceeds to the mixed aminal/carbinolamine 4, such a product would be expected to be in equilibrium with the alternate aminal 5, the latter would be expected to predominate because of the greater stability of aldehyde aminals over the corresponding ketone derivatives. Air oxidation of the tetrahydroimidazole to the imidazoline will then remove 5 from the equilibrium, there is thus obtained the anorectic agent mazindol

7.
Oxprenolol
–
Oxprenolol is a non-selective beta blocker with some intrinsic sympathomimetic activity. It is used for the treatment of angina pectoris, abnormal heart rhythms, oxprenolol is a lipophilic beta blocker which passes the blood–brain barrier more easily than water-soluble beta blockers. As such, it is associated with an incidence of CNS-related side effects than hydrophilic ligands such as atenolol, sotalol and nadolol. Oxprenolol is a compound, the beta blocker is used as a racemate. Analytical methods for the separation and quantification of --oxprenolol and --oxprenolol in urine and in pharmaceutical formulations have been described in the literature

8.
RTI-31
–
-2β-Carbomethoxy-3β-tropane is a synthetic analog of cocaine that acts as a stimulant. Semi-synthesis of this compound is dependent upon the availability of cocaine starting material, according to the article, RTI-31 is 64 x the strength of cocaine in terms of its potency to elicit self-administration in monkeys. WIN35428 was 6 x weaker than RTI-31, whereas RTI-51 was 2.6 x weaker than RTI-31, a further advantage, in addition to potency of this compound, is that its duration of activity is longer than for cocaine. It could therefore be considered within the context as an agonist based therapy for treating cocaine addiction, RTI-31 is already completely psychoactive in its own right meaning that further chemical manipulation should be viewed as an option that is not strictly necessary. RTI-336 is actually made using RTI-31 as starting material, RTI-31 is not an entirely selective DRI in that it also has appreciable SERT and NET blocking affinity. RTI-31 can easily be cleaned though, as is done, for instance, the binding ligand affinities for the different transporters is skewed somewhat in favor of the DAT, there may be some bias in the data. The reason for this could be that WIN35428 is relatively easier to displace from the DAT versus paroxetine from the SERT, also it needs to be borne in mind the idea of transporter promiscuity. It may be possible that the NE levels are raised, at least in part, RTI-31 lies somewhere in the middle of the table between troparil on one end and RTI-55 on the other. It is not as selective as RTI-113 for the DAT, but is more selective than Dichloropane is for this transporter, RTI-31 also has some muscarinic acetylcholine agonist activity. Data in Above table from rats brains, more recent work has advocated using cloned human transporters. Reduced ester to alcohol is called RTI-93, rTI-145 is a methyl carbonate of the alcohol. Conversion of ester in RTI-31 to heteroaromatic nuclei also possible, rTI-470 was among the potent DRI known to exist,0. 094nM. Further chemical modification of RTI-31 leads to novel chemical entities, some of them are highly potent and this is because of the compounds increased lipophilicity. The act of changing a drugs duration of action through altering its lipophilicity is commonly observed, if read nocaine, interesting n-propyl group chosen, -CPCA RTI-336 RTI-113

9.
RTI-51
–
-2β-Carbomethoxy-3β-tropane is a semi-synthetic alkaloid in the phenyltropane group of psychostimulant compounds. First publicized in the 1990s, it has not been used enough to have gained a fully established profile, RTI-51 can be expected to have properties lying somewhere in between RTI-31 and RTI-55. Importantly it has a ratio of monoamine reuptake inhibition of D > S > N which is a balance of effects not produced by other commonly used compounds. It has been used in its 76Br radiolabelled form to map the distribution of dopamine transporters in the brain, modern research seems to confirm the above hypothesis. However, earlier work produced more scattered results, based upon what is obvious from the table, RTI-31, RTI-51, and RTI-55 are all similarly potent TRIs. Data in Above table from rats brains, more recent work has advocated using cloned human transporter/s

10.
RTI-55
–
RTI-55 is a phenyltropane-based psychostimulant used in scientific research and with some medical application/s. This drug was first cited in 1991, RTI-55 is a non-selective dopamine reuptake inhibitor derived from methylecgonidine. However, more selective analogs are derived by conversion to pyrrolidinoamido RTI-229, due to the large bulbous nature of the weakly electron withdrawing iodo halogen atom, RTI-55 is the most strongly serotonergic of the simple para-substituted troparil based analogs. In rodents RTI-55 actually caused death at a dosage of 100 mg/kg, whereas RTI-51 and this observation serves to highlight the disparities that can arise between studies. Although RTI-55 wasnt specifically examined in this study the number of responses in a given session was of the order cocaine > WIN35428 > RTI-31 > RTI-51. If desired, a source of iodine can be utilized. I123 and I125 in particular because these are high energy γ-ray emitters. Compared to the WIN compounds, extremely low Ki values are attainable, RTI-55 is mainly used in scientific research into the dopamine reuptake transporter. Various radiolabelled forms of RTI-55 are used in humans and animals to map the distribution of dopamine transporters and serotonin transporters in the brain. The 123I derivative is known as iometopane, RTI-55 is made as follows, RTI-121 RTI-229 RTI-352 List of Phenyltropanes

11.
RTI-121
–
-2β-Carboisopropoxy-3β-tropane is a stimulant drug used in scientific research, which was developed in the early 1990s. RTI-121 is a phenyltropane based, highly selective dopamine reuptake inhibitor and is derived from methylecgonidine, however RTI-121 occupies the dopamine transporter more slowly than cocaine, and so might have lower abuse potential than cocaine itself. RTI-121 is mainly used in research into the dopamine reuptake transporter. It is more selective for the dopamine transporter than other DAT radioligands such as β-CIT, various radiolabelled forms of RTI-121 are used in both humans and animals to map the distribution of dopamine transporters in the brain. RTI-121 is legal in all throughout the world as of 2007. RTI-55 List of cocaine analogues List of Phenyltropanes

12.
RTI-274
–
RTI-274, or 2β--3α-nortropane is a phenyltropane homologue of paroxetine developed by the group led by F Ivy Carroll in the 1990s. Very few esters of phenyltropanes are actually known to have been reported, nS2330 and NS2359 both have α, β stereochemistry. NS2214 appears to have been abandoned now, RTI-336 was their latest compound, RTI decided that they wanted to make all 8 stereoisomers of the phenyltropane paroxetine homolog. N-demethylating the S-α, β isomer resulted in a 54-fold increase in DAT IC50, in the case of nocaine it is understood that the SR enantiomer is the one that should be demethylated if it is wanted to improve DAT affinity. Interestingly, that is actually the same enantiomer that is used in the production of paroxetine, four years later some unrelated authors cited a skeletal rearrangement accounts for this. Diagram Notice that they are not only interested in ethers, the metal is called Technetium and is bound by a chelating agent. The authors state that at first the acid is halogenated, the amide is prepared, in their case they used a tosyl

13.
Salbutamol
–
Salbutamol, also known as albuterol and marketed as Ventolin among other names, is a medication that opens up the medium and large airways in the lungs. It is used to treat asthma, exercise-induced bronchoconstriction, and chronic pulmonary disease. It may also be used to high blood potassium levels. It is usually used by inhaler or nebulizer but is available as a pill. Onset of action of the version is typically within 15 minutes. Common side effects include shakiness, headache, fast heart rate, dizziness, serious side effects may include worsening bronchospasm, irregular heartbeat, and low blood potassium levels. It can be used during pregnancy and breastfeeding, but safety is not entirely clear, salbutamol is a short-acting β2 adrenergic receptor agonist which works by causing airway smooth muscles to relax. Salbutamol was first made in 1967 in Britain and it was approved for medical use in the United States in 1982. It is on the World Health Organizations List of Essential Medicines and it is available as a generic medication. The wholesale cost in the world of an inhaler which contains 200 doses is between $1.12 and $2.64 as of 2014. In the United States it is between $25 and $50 for a month supply. Salbutamol is typically used to treat bronchospasm, as well as chronic obstructive pulmonary disease, as a β2 agonist, salbutamol also finds use in obstetrics. Intravenous salbutamol can be used as a tocolytic to relax the smooth muscle to delay premature labor. Salbutamol has been used to treat acute hyperkalemia, as it stimulates potassium flow into cells thus lowering the level in the blood, the most common side effects are fine tremor, anxiety, headache, muscle cramps, dry mouth, and palpitation. Other symptoms may include tachycardia, arrhythmia, flushing, myocardial ischemia, rarely occurring, but of importance, are allergic reactions of paradoxical bronchospasm, urticaria, angioedema, hypotension, and collapse. High doses or prolonged use may cause hypokalaemia, which is of concern especially in patients with renal failure and this drug is sold as a racemic mixture. With regard to structure-activity relationships, the tertiary butyl group in salbutamol makes it selective for β2 receptors. Salbutamol may be quantified in blood or plasma, practical needs for this include to confirm a diagnosis of poisoning in hospitalized patients, or to aid in a forensic investigation

14.
Tesofensine
–
Tesofensine is a serotonin–noradrenaline–dopamine reuptake inhibitor from the phenyltropane family of drugs, which is being developed for the treatment of obesity. Tesofensine was originally developed by a Danish biotechnology company, NeuroSearch, as of 2015, tesofensine has been discontinued for the treatment of Alzheimers disease, Parkinsons disease and is in Phase II clinical trials for obesity. However, weight loss was reported as an adverse event in the original studies. Therefore, it was decided to pursue development of tesofensine for the treatment of obesity, Tesofensine primarily acts as an appetite suppressant, but possibly also acts by increasing resting energy expenditure. Phase 2 trials for the treatment of obesity have been successfully completed, Tesofensine has a long half-life of about 9 days and is mainly metabolized by cytochrome P4503A4 to its desalkyl metabolite M1 NS2360. NS2360 is the only metabolite detectable in human plasma, nS2330 is mainly metabolized by cytochrome P450 3A4 into. It has a longer half-life than tesofensine, i. e. approximately 16 days in humans, in vivo data indicate that NS2360 is responsible for approximately 6% of the activity of tesofensine. As in animals, the kidney appears to only a minor role in the clearance of tesofensine in humans. Originally it had reported that Tesofensine has IC50 of 8.0,3.2 and 11. 0nM at the DAT, NAT. More recently, though, the data was submitted, IC50 NE1.7, SER11. The revised IC50s would adequately explain the lack of efficacy in treating PD, i. e. insufficient DRI potency relative to the SERT, Tesofensine also indirectly potentiates cholinergic neurotransmission proven to have beneficial effects on cognition, particularly in learning and memory. Sustained treatment with tesofensine has been shown to increase BDNF levels in the brain, Phase 2b trial results reported in The Lancet showed levels of weight loss over a 6-month period that were significantly greater than those achieved with any currently available drugs. Patients lost an average of 12.8 kg on the 1 mg dose,11.3 kg on the 0.5 mg dose and 6.7 kg on the 0.25 mg dose, compared with a 2.2 kg loss in the placebo group. All participants were instructed to follow a diet with a 300 kcal deficit, the placebo-subtracted mean weight losses were 4. 5%,9. 2% and 10. 6% in the 0.25 mg,0.5 mg and 1 mg dose groups, respectively. This is approximately twice the weight loss produced by medications currently approved by the US Food, all were initially treated with 0.5 mg tesofensine once daily but up-titration to 1.0 mg once daily was allowed in the first 24 weeks of the extension study. At this time point, all subjects were continued on the 0.5 mg dose for an additional 24 weeks. The 24-week interim results for those who were treated with tesofensine 0.5 mg in TIPO-1 showed a total mean weight loss of between 13 kg and 14 kg over 48 weeks of treatment. Furthermore, TIPO-4 confirmed the TIPO-1 results since those patients who were treated with placebo lost approximately 9 kg in the first 24 weeks of the TIPO-4 study

15.
Troparil
–
Troparil is a stimulant drug used in scientific research. Troparil is a dopamine reuptake inhibitor that is derived from methylecgonidine. The lack of an ester linkage removes the local anesthetic action from the drug and this change in activity also makes troparil slightly less cardiotoxic than cocaine. The most commonly used form of troparil is the tartrate salt, the first known published synthesis of troparil and the related compound WIN35428 is by Clarke and co-workers during the 1970s. Apparently, it was their intention to separate the stimulant actions of cocaine from its toxicity, troparil is the only regular phenyltropane having a NET affinity that exceeds the DAT affinity. Phenyltropanes are likely to have less abuse and dependency compared with cocaine, troparil is used in scientific research into the dopamine reuptake transporter. 3H-radiolabelled forms of troparil have been used in humans and animals to map the distribution of dopamine transporters in the brain. It is also used for research into stimulant drugs as an alternative to cocaine which produces similar effects. Troparil has similar effects to cocaine in animal studies, but recreational use of this compound to date has proven extremely rare. The legal status of troparil is unclear, but it may be considered a controlled substance analog of cocaine in the United States on the grounds of its chemical structure. List of phenyltropanes List of cocaine analogues Amfonelic acid

16.
WIN-35428
–
-2-β-Carbomethoxy-3-β-tropane is a stimulant drug used in scientific research. CFT is a phenyltropane based dopamine reuptake inhibitor and is derived from cocaine. It is around 3-10x more potent than cocaine and lasts around 7 times longer based on animal studies, the tartrate is another salt form that is reported. CFT was first reported by Clarke and co-workers in 1973 and this drug is known to function as a positive reinforcer. Tritiated CFT is frequently used to map binding of ligands to the DAT. Radiolabelled forms of CFT have been used in humans and animals to map the distribution of dopamine transporters in the brain. CFT was found to be useful for this application as a normal fluorine atom can be substituted with the radioactive isotope 18F which is widely used in Positron emission tomography. CFT is about as addictive as cocaine in animal studies, but is less often due to its longer duration of action. Potentially this could make it a drug to be used as a substitute for cocaine. In August 2010, some sources claimed that the designer drug Ivory Wave contained WIN35,428. However, samples of Ivory Wave have been found to contain MDPV, administering 100 mg/kg of CFT to rats only resulted in convulsions being reported, whereas CIT had the ability to cause death at this dose. WIN35, 065-2 List of phenyltropanes List of cocaine analogues DMello GD, Goldberg DM, Goldberg SR, conditioned taste aversion and operant behaviour in rats, effects of cocaine and a cocaine analogue. Sershen H, Lajtha A. Saturable cocaine binding in central nervous system of mouse, spealman, RD, Bergman, J, Madras, BK. Self-administration of the high-affinity cocaine analog 2 beta-carbomethoxy-3 beta-tropane, milius, RA, Saha, JK, Madras, BK, Neumeyer, JL. Synthesis and Receptor Binding of N-Substituted Tropane Derivatives, high- Affinity Ligands for the Cocaine Receptor. Cline, EJ, Scheffel, U, Boja, JW, Carroll, FI, Katz, JL, Kuhar, behavioral effects of novel cocaine analogs, a comparison with in vivo receptor binding potency. Journal of Pharmacology and Experimental Therapeutics, singh S. Chemistry, Design, and Structure-Activity Relationship of Cocaine Antagonists. 100, 925-1024 Li, SM, Campbell, BL, Katz, interactions of cocaine with dopamine uptake inhibitors or dopamine releasers in rats discriminating cocaine